The Obesity Code (2016), Jason Fung

I read this at the end of 2018, and it galvanized me on a path of personal change and continual learning about health and wellness. That space has exploded in recent years, especially in the age of podcasts and social media we’re in, and there’s been more research since, but this book was my trailblazer, and what follows are some notes – by a non-physician and neophyte to the material, so keep that caveat in mind – I made for myself back then.

Just educating myself a little more about how our bodies – the most important thing we have – function, felt empowering, and it was also surprising, given what I thought I knew already. I still find it somewhat shocking that fasting, something that barely crosses our minds, so simple as to be banal, can be so transformative. The Diabetes Code, by the same author, is similarly excellent.

Obesity as an epidemic is recent, only materializing in the last generation. It began in the 1950’s, as a function of increased life expectancy: the average age of the first heart attack is 66 years, and more people were reaching this age. Cholesterol was thought to cause heart disease, and dietary fat was thought to increase cholesterol, so physicians advocated lower-fat diets, which in turn increased carbohydrate intake. In 1977, a government committee (not a committee of physicians) introduced the Food Pyramid, advocating less fat and more carbohydrates, and the rates of obesity started increasing from that very year. Because refined carbohydrates couldn’t be both good (low in fat) and bad (fattening), it was decided that they weren’t fattening, and instead, excess calories were to blame.

The two variables – Calories Input, Calories Output – are independent of each other. Output is actually dependent on Input – if you reduce your caloric intake by 30%, your body adjusts to reduce its output by 30%. Our hormones ensure that these two variables stay synchronized with each other.

Basal Metabolic Rate (BMR), the calories your body uses to maintain essential functions, is stable. In fact, your body adjusts its BMR up or down based on the calories available to it.

We can consciously control Calories Input. Our hormonal systems actually influence when to start and stop eating; body-fat regulation is under automatic control.

Fat stores are unregulated, so that eating causes fat. In fact, our hormones control fat creation in our bodies, based on food intake and activity levels.

A calorie is a calorie – that is, all calories are created equal. However, different foods affect our hormonal systems differently, and it is hormones that control fat creation, so calorie counts aren’t actually that meaningful. Different types of calories cause different metabolic responses – for example, some types heat the body, while others cause the body to deposit fat.

Studies repeatedly show no correlation between caloric consumption and weight gain: caloric reduction is not the primary factor in weight loss. If the body has more calories to work with, it will automatically use them. Fat accumulation is a problem of misdirected energy expenditure, too much diverted to fat creation instead of other functions, for example, body-heat production. Conversely, if you reduce calories, your body simply reduces expenditure – on heating the body, maintaining blood pressure, pumping the heart, etc. Studies also show no association between activity and obesity, because increasing exercise, or caloric expenditure, simply results in your body adjusting other activities to compensate, for example, decreasing BMR.

There seems to be a preferred point for body weight and fatness, and overeating and undereating triggers mechanisms to defend against weight change. The problem with obesity is that this preferred point is set too high because of hormonal imbalance, and this is why diets ultimately fail.

Insulin

Hormones are signalling molecules that attach to target cells by binding to their specific receptor – for example, insulin to the insulin receptor, signalling the cell to allow glucose – blood sugar – to enter. Insulin is a hormone that regulates metabolism, allowing cells to use glucose for short term energy, and also promoting fat storage for future energy use.

During mealtimes, ingested carbs lead to excess glucose, and insulin is released to remove this flood of glucose by storing it as glycogen, a short term energy store, in the liver. However, liver space is limited, and once full, further excess carbs are stored as fat, the long term energy store. During a short term fast – for example, after a meal – the liver breaks down glycogen into glucose for energy. And during a prolonged fast, after glycogen stores are exhausted, new glucose is made from the fat stores via fat burning. So, eating triggers an insulin response, and when we fast, insulin goes down.

Administering high doses of insulin in Type 1 and Type 2 diabetes patients is associated with major weight gain, even with lower caloric intake. Type 1 diabetics are unable to produce normal amounts of insulin, and the hallmark of this condition is severe weight loss. People with insulinomas, rare insulin-secreting tumors that produce large amounts of insulin, suffer from weight gain, but immediately lose the weight upon removal of the tumors. Obese patients exhibit a higher fasting insulin level and an exaggerated insulin response to food. In all of this, high levels of insulin are associated with weight gain: the key question is how to reduce insulin.

Insulin Resistance

The major pathway to increased insulin – insulin resistance – is time dependent; like obesity, it takes years to become insulin resistant. In insulin resistance, the insulin receptors stop binding as well as they used to, and more insulin is needed to clear glucose from the bloodstream.

In nature, resistance often is the result of overexposure – antibiotic resistance occurs because antibiotic drugs are taken too often, so more and more resistant organisms survive over time and eventually dominate. Similarly, a vaccine works by exposing the body to small doses of a virus – viruses cause viral resistance. The efficacy of drugs – alcohol, narcotics, caffeine – decreases with increasing use, as the body reacts by decreasing its number of receptors. Resistance is caused by a self-reinforcing, vicious cycle, and it is insulin that causes insulin resistance.

The body is exposed to high hormone levels, but usually as a burst immediately followed by very low levels – for example, melatonin spikes at night to help us sleep, and cortisol early in the morning to wake us up – so that resistance never develops. However, when we snack through the day, especially on refined carbs, the body never gets a chance to rest from insulin, and insulin resistance results. Insulin resistance leads to higher fasting insulin levels, which is the time when the receptors should be getting a break, leading to a classic vicious cycle.

This explains studies that show eating small frequent meals does not aid weight loss, control hunger, or reduce blood glucose. As eating norms changed over time from “eat three meals, no snacks” to make snacking socially acceptable, so did obesity rates.

Food, Fructose, Fiber

Snack food was invented and promoted to make more money: processed foods with flour and sugar don’t spoil, which dramatically reduces costs. Big Food sponsored medical associations to get endorsements (eg. the AHA check mark), and promoted calories as the scapegoat for obesity instead of refined carbs. Big Food especially loves breakfast, but when we wake the body’s natural circadian rhythm spikes us with cortisol, growth hormone, and other hormones, so that we are ready for action and don’t need immediate fuel. Studies show breakfast eating is not correlated to weight loss, and tends to be associated with eating more throughout the day. If you’re not hungry, don’t eat.

The rising obesity rate also parallels sugar consumption from 1977-2000, with a 10 year lag. The worst offender is sugar-sweetened drinks like soda, sweetened iced teas, and sport drinks. Type 2 diabetes is the disease of extremely high insulin resistance, and both obesity and Type 2 diabetes share the root cause of excess insulin. Companies focused on Asia after North America started reducing its sugar consumption, and today, Asian sugar consumption is rising at 5% a year, while the adult type 2 diabetes rate in China (11.6%) is higher than in the US (11.2%) – in 1980, it was only 1%.

Sugar stimulates insulin, as do most refined carbs like rice and potatoes, but sugar is especially bad because of fructose, another sugar like glucose, found naturally in fruit. Table sugar, or sucrose, is composed of 50% glucose and 50% fructose, while high fructose corn syrup (HCFS) is 45% glucose, 55% fructose. While fruit only contributes small amounts of fructose to our diet, HFCS dramatically increased it – it is found in almost every processed food, given its low cost, and the rise in obesity mirrors the rise in HFCS.

The problem with fructose is that it can only be metabolized in the liver and does not circulate in blood; the brain and muscles cannot use it directly for energy. Excess fructose puts pressure on the liver, because no other organ can help; there, it is converted into fat, causing fatty liver, a precursor to type 2 diabetes. If the liver is already full of fat, insulin has more difficulty forcing food energy into the liver, so that higher levels of insulin are needed, causing eventual insulin resistance, usually over years.

While refined carbs (sugar, flour) cause the greatest increase in insulin, not all carbs are bad. Refined carbs purify and concentrate the carb, removing fat, fiber and protein and causing the carb to be digested and absorbed very quickly, spiking glucose and insulin levels, and encouraging overconsumption because the fiber and bulk associated with satiety (fullness) has been removed. Conversely, whole grains are protective against obesity and diabetes, because the fiber they contain increases satiety and slows down the rise of glucose and insulin by reducing the absorption and digestion of food.

Protein

Certain nutrients are considered essential because our bodies cannot synthesize them, and without them, our health suffers; certain fats and proteins fall into this category. However there are no essential carbs or sugars, and carbs are not required for survival – with this insight, the Atkins diet was born.

The Atkins diet had a high-protein component, but while protein does not raise glucose, dietary protein causes a surge in insulin comparable to refined carbs. Multiple glucose-independent pathways of insulin release exist – for example, the cephalic phase is when the body anticipates food as soon as it enters your mouth, so that swishing a sucrose solution and spitting it out will increase your insulin level. High-protein foods can cause weight gain because of insulin stimulation, so replacing carbs with protein may not always be as beneficial as thought – a large European study (1997) showed meat intake significantly associated with weight gain. However, note that vegetable proteins raise insulin only minimally, and that pure fats like olive oil do not stimulate insulin, although fatty foods containing protein can do so.

Fats

Nutritional orthodoxy from 1977 was that dietary fat clogged up arteries and caused heart attacks: high cholesterol came from saturated fats, and this cholesterol deposits on arteries, causing heart disease. Today, we know that heart disease is caused by atherosclerosis, where the heart’s arteries narrow and harden because of plaque buildup. It is thought that plaque develops because inflammation allows cholesterol and inflammatory cells into the artery walls, so that heart attacks and strokes are predominantly inflammatory diseases, rather than simple diseases of high cholesterol. As for cholesterol, it is the liver that produces 80% of the cholesterol in your blood, with only 20% coming from food. Cholesterol is a key building block in our cell membranes, and every cell in the body except for the brain can make it; if you reduce cholesterol in your diet, your body simply makes more.

While dietary fats were demonized by the Food Pyramid in 1977, today, the reputation of saturated fats has been rehabilitated with recent large studies. No association has been found between dietary fat and obesity. Eating fat does not make you fat, but may protect you from it, since eating fat with other foods tends to decrease glucose and insulin spikes.

What to Eat

Saying to eat in moderation is not helpful, because there are certain foods that must be severely restricted (sodas, candy), and others that do not need restriction at all (kale, broccoli). The rational therapy is to lower insulin levels.

Reduce consumption of added sugars:

Remove the sugar bowl and candy.

Read food labels, recognizing the pseudonyms for sugar.

Just don’t snack. The healthy snack is one of the greatest weight-loss deceptions; as recently as the 60s, most people just ate 3 meals a day. Constant stimulation of insulin eventually leads to insulin resistance.

Insulin resistance is a problem of meal timing: to break the insulin resistance cycle, we must have recurrent periods of very low insulin levels, mimicking our natural hormonal cycle of high spikes followed by low periods. If all foods raise insulin to some level, to lower insulin we need to completely abstain from food – that is, fast. While starvation is the involuntary, uncontrolled absence of food, fasting is the voluntary abstinence from food for spiritual, health or other reasons, and has a long recorded history.

The body uses glucose and fat for fuel – when glucose or food runs out, the body transitions to using fat for energy, undergoing the following stages:

Feeding – insulin levels rise, and glucose is used for energy, with any excess stored as glycogen in the liver.

Ketosis (1-3 days) – stored fat (triglycerides) is broken into glycerol (converted into glucose), and fatty acids. These fatty acids are used directly for energy by many tissues, and also converted into ketone bodies for use by the brain, accounting for up to 75% of its energy requirements.

Fasting is the most efficient way to decrease insulin levels, and can be seen in fasting periods as short as 24-36 hours, with longer fasts seeing more dramatic reductions. Regular fasting that routinely lowers insulin levels improves insulin sensitivity, something diets cannot do. Because insulin causes salt and water retention in the kidney, lowering insulin rids the body of excess salt and water – diuresis – which also reduces bloating.

Growth hormone increases the availability and utility of fats for fuel, and helps preserve muscle mass and bone density. While it is normally released intermittently and decreases with age, over a 5 day fast, growth hormone secretion more than doubles to maintain muscle and bone tissue mass.

Fasting increases adrenaline starting after 24 hours, so that after 48 hours the metabolic rate increases by 3.6%, and after 4 days, 14% – presumably to supply the energy to find more food.

Electrolytes remain stable during fasting, although a multivitamin supplement will provide the daily recommended allowance of micronutrients.

Fasting myths that demonize fasting ignore the fact that we would never have survived as a species if the body could not rely on its energy stores (as fat) during times of scarcity.